Infant outcome after prenatal exposure to antiepileptic compounds is of considerable concern to women with epilepsy. Under most circumstances, it would be detrimental to the woman's health, and perhaps that of the fetus, to have the medication withdrawn during pregnancy. At the same time, there is risk to the fetus exposed to antiepileptic compounds, and minimizing teratogenicity (e.g., growth problems and postnatal developmental delays) is of considerable importance. Carbamazepine (CBZ Tegretol() is currently the drug of choice in temporal lobe epilepsy and has been used as an alternative to phenytoin (PHT Dilantin(), which is known to induce teratogenicity. Although little is known about the actual mechanism of CBZ teratogenicity, oxidative metabolism has been implicated. Oxcarbazepine (OCBZ Trileptol(), an experimental compound in the U.S. (currently in clinical use in Europe), seems to be as efficacious as CBZ and has been suggested as a substitute for CBZ owing to its greater tolerability by patients. OCBZ is metabolized via reduction to form a monohydroxy derivative, whereas CBZ is oxidized to form an epoxide. This difference avoids the formation of reactive arene oxides and epoxides possibly responsible for the teratogenicity of CBZ. However, the potential liability of OCBZ to prenatally exposed infants is completely unknown. The goal of this research project is to test the teratogenicity of oxcarbazepine in a monkey model. To date, 15 females and 3 breeder males are on study. Nine of the animals are on preliminary kinetics studies to determine the OCBZ dosing design for the pregnancy studies. The remaining six animals are on a CBZ or control regimen and will produce infants that will be compared with OCBZ-exposed infants in the postnatal studies. Two infants are due to be born in February 1998.